ABSTRACT
Objective To observe the changes of water, potassium and sodium in the hypoxic cerebral tissues in mice and the effects of progesterone on the tissues and investigate the neuroprotective role of progesterone (PROG)in the cerebral anoxia. Methods Thirty - two male mice were divided into control group, simple hypoxia group, lower dosage group and higher dosage group. Progesterone was injected intraperitoneally in the dosage of 4 mg/kg or 8 mg/kg respectively 30 min before hypoxia in the last two groups. The contents of water, potassium and sodium in brain tissues in mice were evaluated at 24 hours after cerebral anoxia. Results The water, potassium and sodium contents in simple hypoxia group were significantly higher than those in control group(P0.05)in higher dosage group(8 mg/kg PROG)compared with those of simple hypoxia group. Conclusions At 24 hours after cerebral anoxia, there are significant increases of water, potassium and sodium in brain tissues. Progesterone may pro-duce neuroprotective role by inbibiting the rise of them.
ABSTRACT
Objective To study the effects of mild hypothermia on nervous cell apoptosis and activity of Caspase - 3 after hypoxia -ischemia brain damage (HIBD) in neonatal rats. Methods Seven - day SD rats were divided into sham operation group,normothermia HIBD group (HIBD group) and mild hypothermia HIBD group(mild hypothermia group). In HIBD group,the left carotid of rats was ligated and animals were exposed to 8% oxygen for 2 h.and in mild hypothermia group,hypothermia of 31 - 32 1C lasting 8 hours was used just after HIBD. L sing methods of TUNEL and AC - DEVI) - AMC, the apoptotic cell rate and Caspase - 3 activity level were determined in sham operated group, HIBD group and mild hypothermia group separatively. Results The apoptotic cell rate and Caspase - 3 activity level were significantly lower in sham - operated group and mild hypothermia group than those in HIBD group. Conclusion One of the mechanisms of brain protection by mild hypothermia may be contributed to the decrease of neural cell apoptosis and the activity level of Caspase 3 HIBD.